Regulatory T Cells Modulate Staphylococcal Enterotoxin B-Induced Effector T-Cell Activation and Acceleration of Colitis
2009
Heriazon, Armando | Zhou, Pengfei | Borojevic, Rajka | Foerster, Katharina | Streutker, Catherine J. | Ng, Tsun-Ming T. | Croitoru, Kenneth
Oral administration of bacterial superantigen Staphylococcus aureus enterotoxin B (SEB) activates mucosal T cells but does not cause mucosal inflammation. We examined the effect of oral SEB on the development of mucosal inflammation in mice in the absence of regulatory T (Treg) cells. SCID mice were fed SEB 3 and 7 days after reconstitution with CD4⁺ CD45RBhigh or CD4⁺ CD45RBhigh plus CD4⁺ CD45RBlow T cells. Mice were sacrificed at different time points to examine changes in tissue damage and in T-cell phenotypes. Feeding SEB failed to produce any clinical effect on SCID mice reconstituted with CD4⁺ CD45RBhigh and CD4⁺ CD45RBlow T cells, but feeding SEB accelerated the development of colitis in SCID mice reconstituted with CD4⁺ CD45RBhigh T cells alone. The latter was associated with an increase in the number of CD4⁺ Vβ8⁺ T cells expressing CD69 and a significantly lower number of CD4⁺ CD25⁺ Foxp3⁺ T cells. These changes were not observed in SCID mice reconstituted with both CD45RBhigh and CD45RBlow T cells. In addition, SEB impaired the development of Treg cells in the SCID mice reconstituted with CD4⁺ CD45RBhigh T cells alone but had no direct effect on Treg cells. In the absence of Treg cells, feeding SEB induced activation of mucosal T cells and accelerated the development of colitis. This suggests that Treg cells prevent SEB-induced mucosal inflammation through modulation of SEB-induced T-cell activation.
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